Objective Local immunity plays an important role in the cervical defense mechanisms that prevent the development of cervical intraepithelial neoplasia. The objective of this study was to determine the involvement of local immunity by evaluating Langerhans cell (LC) density in cervical biopsies of human immunodeficiency virus (HIV)-positive and HIV-negative women.
Materials and Methods A cross-sectional study was developed by including HIV-positive and HIV-negative women. All patients presented human papillomavirus DNA from the uterine cervix, which was detected by polymerase chain reaction or hybrid capture II. Cervical biopsies were assessed for LC density and cervical intraepithelial neoplasia. Langerhans cells were identified by immunohistochemistry using anti-CD1a and anti-S100 antibodies. Associations among cervical LC density, the type of cervical lesion, CD4+ lymphocyte count, and HIV viral load were analyzed using logistic regression (SPSS, version 12.0).
Results Seventy-seven women (40 seropositive and 37 seronegative) were enrolled. The mean ± SD LC density identified with the anti-CD1a antibody was 0.80 ± 0.7 cells versus 2.6 ± 1.6 cells (P < 0.0001), whereas the mean ± SD LC density identified by the anti-S100 antibody was 1.3 ± 1.0 cells versus 3.6 ± 1.7 cells (P < 0.0001) among the HIV-positive and HIV-negative women, respectively. There were no associations between LC density and HIV viral load, CD4+ lymphocyte count, or human papillomavirus genotype (P > 0.05). In a logistic regression model, HIV infection was the only factor independently associated with a decrease in LC density.
Conclusions Human immunodeficiency virus infection was found to be an independent factor that explains the decrease in local immunity in the uterine cervix, which could allow the development of cervical lesions. This effect was not associated with CD4+ lymphocyte count or HIV viral load.
- cervical intraepithelial neoplasia
- viral load
- human papillomavirus
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The authors declare no conflicts of interest.
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